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A growth trial was conducted to evaluate the effects of dietary lipid levels on the lipid deposition and metabolism of subadult triploid rainbow trout. Diets with low (148 g lipid kg-1 diet), moderate (228 g lipid kg-1 diet), and high (294 g lipid kg-1 diet) crude lipid contents were fed to quadruplicated groups of fish ( 233   g ± 0.2   g ) for 80 days, and they were named as LL, ML, and HL, respectively. Results showed that the lowest and highest values of condition factor and hepatosomatic index were shown in the LL group, respectively, while the HL group obtained the highest liver redness value, plasma total cholesterol, high-density lipoprotein-cholesterol, and low-density lipoprotein-cholesterol contents ( P < 0.05 ). The viscerosomatic index and plasm glucose, nonesterified fatty acids, and triglyceride contents were comparable among groups ( P > 0.05 ). As for lipid deposition, viscera and muscle were the main lipid storage place for triploid rainbow trout when tissues’ weight is taken into consideration. Overall quantitative PCR showed that the lipid uptake, triglyceride, and fatty acid catabolism were upregulated, but glycolysis was downregulated as dietary lipid increased. The expression of genes involved in lipogenesis, lipoprotein clearance, very low-density lipoprotein assembly, and glycogenesis was not affected by dietary lipid levels ( P > 0.05 ). In summary, subadult triploid rainbow trout store lipid mainly in viscera and muscle; it could maintain hepatic lipid homeostasis when fed with dietary lipid levels ranging from 150 to 300 g kg-1 by regulating lipid uptake and switching energy supply between glycolysis and fatty acids β-oxidation.

This experiment simulated the hypoxic environment caused by actual production operations in fish farming (i.e., catching, gathering, transferring, and weighting) to study the effects of acute hypoxic conditions on the physiological and metabolic responses of triploid rainbow trout (O. mykiss). Two groups of fish weighting 590 g were sampled in the normoxia group (dissolved oxygen above 7 mg/L) and hypoxia group (dissolved oxygen ranged from 2 to 5 mg/L for 10 min). The results showed that 1) regarding stress response, hypoxia increased plasma levels of cortisol, heat shock protein 70 (HSP-70), lysozyme, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and creatine phosphokinase (CPK); induced the expression of hepatic genes encoding nuclear factor erythroid 2 related factor 2 (Nrf2), interferon γ (IFN-γ) and interleukin-1β (IL-1β). 2) Regarding metabolism response, hypoxia increased plasma levels of globulin (GLOB), glucose (GLU), triglyceride (TG) and lactate dehydrogenase (LDH); upregulated the hepatic gene expression of phosphoenolpyruvate carboxykinase, (PEPCK), pyruvate dehydrogenase kinase (PDK1), acetyl-CoA carboxylase (ACC) and acetyl-CoA oxidase (ACO); downregulated the hepatic gene expression of carnitine palmitoyl transferase 1 (CPT1); and unchanged the expression of hepatic genes in glycolysis and autophagy. 3) In response to hypoxia-inducible factors (HIFs), the hepatic HIF-2α gene was activated in the hypoxia group, but HIF-1α gene expression remained unchanged. Thus, during acute hypoxic stress, triploid rainbow trout were in a defensive state, with an enhanced immune response and altered antioxidant status. Additionally, the hepatic mitochondrial oxidation of glucose- and lipid-derived carbon in trout was suppressed, and hepatic gluconeogenesis and lipid synthesis were activated, which might be regulated by the HIF-2α pathway.

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